Role of macrophage scavenger receptor 1 in the progression of dyslipidemia in acne vulgaris patients

Abstract

AbstractBackgroundMacrophage scavenger receptor 1 gene (MSR1), is responsible for producing macrophage scavenger receptors. MSR1 is primarily located on the surfaces of various macrophage types and is known to exert a range of effects on the human body. These effects include influencing innate and adaptive immunological reactions, as well as contributing to the development of conditions such as atherosclerosis, dyslipidemia, liver and lung disease, and cancer. The unregulated assimilation of lipoproteins by MSR1 leads to the creation of macrophages rich in cholesterol that manifest as foam‐like cells, ultimately contributing to dyslipidemia. This occurrence highlights the significance of MSR1 as a key player in the pathophysiology of dyslipidemia.AimIn this study, we aimed to estimate variation in lipid profile in acne vulgaris (AV) patients. Also, we aimed to investigate the role of MSR1 in lipid profile variation.Subjects and methodsA case‐control study consisting of 100 patients with AV and 104 healthy controls. Lipid profiles were assessed using normalized enzymatic processes and genotype analyses were performed by a polymerase chain reaction and standard Sanger sequencing. Predictions of variant effects were performed using in silico tools.ResultOur results indicated that the levels of lipid profile were higher in patients with AV than in healthy patients. The two haplotypes that were most prevalent in the patients were TCAC (16.5%) and CAGG (15.47%), whereas the two haplotypes that were more prevalent in the controls were TAAC (16.43%) and CCAC (15.62%). IVS5.59 C > A and rs433235 A > G are in linkage disequilibrium. Additionally, rs433235 A > G has a significant linkage disequilibrium with rs3747531 C > G. In silico analysis, tools indicated that the rs433235 A > G variant was disease‐causing.ConclusionPatients diagnosed with TCAC and CAGG exhibited a higher prevalence compared to healthy patients with TAAC and CCAC. The linkage disequilibrium between rs433235 A > G and IVS5.59 C > A has been established. Furthermore, there appears to be significant linkage disequilibrium between rs3747531 C > G and rs433235 A > G. These findings support the notion that genetic variations may play a critical role in the pathogenesis of these conditions.